Download Cardiovascular Physiology

Cardiovascular
Physiology
Dr. Khalid Alregaiey
Gross Anatomy of Heart: Frontal Section
Pathway of Blood Through the Heart and Lungs
• Right atrium  tricuspid valve  right ventricle
• Right ventricle  pulmonary semilunar valve 
pulmonary arteries  lungs
• Lungs  pulmonary veins  left atrium
• Left atrium  bicuspid valve  left ventricle
• Left ventricle  aortic semilunar valve  aorta
• Aorta  systemic circulation
Pathway of Blood Through the Heart and Lungs
The Sectional Anatomy of the Heart
The Sectional Anatomy of the Heart
Heart chambers and valves
• Structural Differences in heart chambers
• The left side of the heart is more muscular than
the right side
• Functions of valves
• AV valves prevent backflow of blood from the
ventricles to the atria
• Semilunar valves prevent backflow into the
ventricles from the pulmonary trunk and aorta
Atrioventricular Valve Function
Semilunar Valve Function
Cardiac Physiology
• Two classes of cardiac muscle cells
• Specialized muscle cells of the conducting
system
• Contractile cells
The Conducting System of The Heart
• The conducting system includes:
• Sinoatrial (SA) node (pacemaker)
• Atrioventricular (AV) node
• atrioventricular bundle (bundle of His)
• Purkinje fibers
The Conducting System of The Heart
Impulse Conduction through the heart
• SA node generates impulses about 75
times/minute (pacemaker)
• Stimulus spreads to the AV node
• Impulse is delayed at AV node
• Impulse passes from atria to ventricles via
the atrioventricular bundle (bundle of His)
• Then distributed by Purkinje fibers
Sequence of Excitation
The electrocardiogram (ECG)
• A recording of the electrical events occurring
during the cardiac cycle
• The P wave corresponds to the
depolarization of SA node
• The QRS complex corresponds to
ventricular depolarization
• The T wave corresponds to ventricular
repolarization
An Electrocardiogram
Electrocardiogram (ECG):
• Einthoven's
triangle
• P-Wave –
atria
• QRS- wave –
ventricles
• T-wave –
repolarization
An Electrocardiogram
ECG Information Gained
• (Non-invasive)
• Heart Rate
• Signal conduction
• Heart tissue
• Conditions
Figure 14-24: Normal and abnormal electrocardiograms
Autonomic Innervation of the Heart
Extrinsic Innervation of the Heart
• Heart is stimulated
by the sympathetic
center
• Heart is inhibited
by the
parasympathetic
center
Sympathetic and Parasympathetic
• Sympathetic – speeds heart rate by  Ca++ & I-f
channel flow
• Parasympathetic – slows rate by  K+ efflux & 
Ca++ influx
Heart Excitation Related to ECG
Heart Sounds
• Auscultation – listening to heart sound via
stethoscope
• Four heart sounds
• S1 – “lubb” caused by the closing of the AV
valves
• S2 – “dupp” caused by the closing of the
semilunar valves
• S3 – a faint sound associated with blood
flowing into the ventricles
• S4 – another faint sound associated with atrial
contraction
Cardiac Cycle
• Cardiac cycle refers to all events
associated with blood flow through the
heart
• Systole – contraction of heart muscle
• Diastole – relaxation of heart muscle
Heart Cycle:
1. Late diastole: all chambers relax, filling
with blood
2. Atrial systole: atria contract, add 20%
more blood to ventricles
3. Isovolumic ventricular contraction:
closes AV valves ("lub"), builds pressure
Heart Cycle: Finish and Around To the Start
4. Ventricular ejection: pushes open semi
lunar valves, blood forced out
5. Ventricular relaxation: Backflow of blood
in aorta and pulmonary trunk closes
semilunar valves ("dup")
AV valves open refilling starts – back to
start of cycle
Heart Cycle
Phases of the Cardiac Cycle
Cardiac Output (CO) and Reserve
• CO is the amount of blood pumped by
each ventricle in one minute
• CO = heart rate (HR) X stroke
volume (SV)
• HR is the number of heart beats per
minute
• SV is the amount of blood pumped out by
a ventricle with each beat
• Cardiac reserve is the difference between
resting and maximal CO
Cardiac Output: Example
• CO (ml/min) = HR (75 beats/min) x SV (70
ml/beat)
• CO = 5250 ml/min (5.25 L/min)
Regulation of Stroke Volume
• SV = end diastolic volume (EDV) minus
end systolic volume (ESV)
• EDV = amount of blood collected in a
ventricle during diastole
• ESV = amount of blood remaining in a
ventricle after contraction
Factors Influencing Stroke Volume
• Force of contraction
• Venous return:
• Skeletal pumping
• Respiratory pumping
Regulation of Heart Rate: Autonomic Nervous System
• Heart rate range: about 50 – near 200
• Typical resting: near 70 (60-100).
• Hormones like epinephrine, norepinephrine,
thyroid hormone (T3) increase heart rate.
• Sympathetic stimulation
• Releases norepinephrine (NE)
• Increases heart rate
• Parasympathetic stimulation
• Releases acetylcholine (Ach)
• Decreases heart rate
Regulators of the Heart Rate
Figure 14-28: Reflex control of heart rate
Factors Influencing CO
Blood Flow, Blood Pressure, and Resistance
• Blood flow (F) is directly proportional to the
difference in blood pressure (P) between two
points in the circulation
• If P increases, blood flow speeds up; if P
decreases, blood flow declines
• Blood flow is inversely proportional to resistance
(R)
• If R increases, blood flow decreases
• R is more important than P in influencing local
blood pressure
Systemic Blood Pressure
• The pumping action of the heart generates blood
flow through the vessels along a pressure
gradient, always moving from higher- to lowerpressure areas
• Pressure results when flow is opposed by
resistance
• Systemic pressure:
• Is highest in the aorta
• Declines throughout the length of the pathway
• Is 0 mm Hg in the right atrium
• The steepest change in blood pressure occurs in
the arterioles
Systemic Blood Pressure
Maintaining Blood Pressure
• The main factors influencing blood pressure are:
• Cardiac output (CO)
• Peripheral resistance (PR)
• Blood volume
• Blood pressure = CO x PR
• Blood pressure varies directly with CO, PR, and
blood volume
Chemicals that Increase Blood Pressure
• Adrenal medulla hormones: norepinephrine and
epinephrine increase blood pressure
• Antidiuretic hormone (ADH) – causes intense
vasoconstriction in cases of extremely low BP
• Angiotensin II – kidney release of renin generates
angiotensin II, which causes intense
vasoconstriction
• Endothelium-derived factors – endothelin and
prostaglandin-derived growth factor (PDGF) are
both vasoconstrictors
Chemicals that Decrease Blood Pressure
• Atrial natriuretic peptide (ANP): causes blood
volume and pressure to decline
• Nitric oxide (NO): has brief but potent vasodilator
effects
• Inflammatory chemicals: histamine, prostacyclin,
and kinins are potent vasodilators
• Alcohol: causes BP to drop by inhibiting ADH
Alterations in Blood Pressure
• Hypotension: low BP in which systolic pressure is
below 100 mm Hg
• Hypertension: condition of sustained elevated
arterial pressure of 140/90 or higher
• Transient elevations are normal and can be
caused by fever, physical exertion, and
emotional upset
• Chronic elevation is a major cause of heart
failure, vascular disease, renal failure, and
stroke
Factors Aiding Venous Return
• Venous BP alone is too low to promote adequate
blood return and is aided by the:
• Respiratory “pump” – pressure changes
created during breathing suck blood toward the
heart by squeezing local veins
• Muscular “pump” – contraction of skeletal
muscles “milk” blood toward the heart
• Valves prevent backflow during venous return
The Function of Valves in the Venous System
Capillaries
• Narrowest of vessels; wide enough to allow only
for single file passage of RBCs
• Causes slowest flow rate of any vessels in
system
• Thinnest of vessels; walls composed of a single
cell layer
• No smooth muscle
• No elastic
• More capillaries than all other types of vessels
• Greatest cross-sectional area of all vessels in
system
Capillary Structure
Capillaries (continued)
•
•
•
•
Slowest flow rate
Thinnest walls
Narrowest Diameters
Greatest total cross-sectional area
Optimal conditions for
maximum diffusion of
gases, nutrients and
wastes in capillary beds
Processes that move fluids across capillary walls
• Diffusion
• Filtration
• Hydrostatic pressure (CHP)
• Reabsorption
Forces Acting across Capillary Walls